Macrophage dysregulation is a hallmark of chronic sterile inflammatory diseases including cancer, atherosclerosis, and obesity/type 2 diabetes. Because macrophages are highly influenced by their environment, we need to understand how disease-specific changes to their environment dysregulate specific pathways to drive pathogenesis. Moreover, the relationship between these macrophage pathways to those required for pathogen clearance is largely unknown, which is important because attempts to therapeutically target macrophages must preserve this important function. Comparing and contrasting macrophages across a spectrum of diseases is therefore required to elucidate disease-specific mechanisms, and to develop therapeutics that are both efficacious and safe. To enable this, my lab combines proteomic, bioinformatic, immunologic, and functional approaches to study macrophages in an unbiased manner across a spectrum of diseases.

Our long-term goal is to develop a robust research program that uses a multi-disease approach to develop a comprehensive understanding of macrophage biology, and then translates this mechanistic understanding to develop therapeutics across a spectrum of human disease. To this end, my lab is developing 2 new therapies for the treatment of many cancers and anti-inflammatory therapies that do not interfere with pathogen clearance for treating atherosclerosis and type 2 diabetes.